Delayed Recall Memory Impairment in Patients With Parkinson's Disease

Dement Neuropsychol 2016 September;10(3):204-209
Original Article
doi: 10.1590/S1980-5764-2016DN1003006
Delayed recall memory impairment in

patients with Parkinsons disease
Arthur Oscar Schelp1, Cristiane Lara Mendes-Chiloff2,
Vanessa Cristina Paduan2, Jos Eduardo Corrente3, Fabrcio Diniz de Lima4,
Juliana Cristine Nunes Marchette2, Gustavo Jos Luvizuto5, Rodrigo Bazan1
ABSTRACT. Age is one of the risk factors for dementia in patients with Parkinsons disease (PDD). Distinct cognitive
syndromes of Parkinsons disease (PD) have been identified in previous studies. Questions about the role of such cognitive
disorders in PD outcomes, especially memory dysfunction, in patients with PD remain unanswered. Objective: To
establish possible correlations between delayed recall memory (episodic memory), age, and other demographic variables
in patients with PD. Methods: A two-stage protocol was applied. Patients with delayed recall memory compromise,
selected based on a brief battery of tests (BBRC-Edu), were classified as dementia cases and submitted to the Mattis
Dementia Rating Scale (MDRS). Data from patients with memory disturbances were compared against individuals without
episodic memory impairment, and correlated with age and demographic variables. Results: Except for identification
and naming, all subtests in the screening battery showed a significant difference (p0.0001) between the memorycompromised group (case) and the group without memory impairment (no case). The results also correlated negatively
with age (p0.0001) and positively with level of education (p=0.0874) in patients with PD. Conclusion: The analysis
showed a significant relationship between age and dementia characterized by impaired episodic memory. The findings
support reports of a wide spectrum of neuropsychological performance impairment in PD with age, particularly dementia
associated with memory deterioration. No correlations between disease duration and cognitive dysfunction were evident.
Key words: Parkinsons disease, dementia, ageing.
COMPROMETIMENTO DA MEMRIA DE EVOCAO TARDIA NA DOENA DE PARKINSON
RESUMO. Idade um fator de risco bem determinado para surgimento de demncia em pacientes com doena de
Parkinson (PDD). Estudo prvio tem demonstrado diferentes distrbios cognitivos em portadores da doena de Parkinson
(PD). O significado do comprometimento da memria pouco compreendido. Objetivo: Estabelecer possveis correlaes
entre comprometimento de memria de evocao tardia (memria episdica), idade e outras variveis demogrficas em
pacientes com DP. Mtodos: Os pacientes foram submetidos a um protocolo dividido em duas etapas. Os pacientes
com alteraes na memria de evocao tardia (memria episdica), selecionados a partir de bateria breve de rastreio
cognitivo (BBRC-Edu) foram classificados como portadores de demncia e submetidos ao exame de rastreio para
demncia de Mattis (MDRS). Os dados relacionados a comprometimento da memria, foram comparados ao grupo
que no apresentava alteraes e correlacionados a idade e outras variveis demogrficas. Resultados: Com exceo
de identificao e nominao, todos os sub-testes mostraram diferenas significativas (p0,0001) entre o grupo que
apresentava disfunes na memria episdica e o grupo que no apresentava alteraes. Foi demonstrada correlao
negativa com idade (p0,0001) e positiva com nvel educacional (p=0.0874). Concluso: O estudo registrou correlao
significativa entre idade e demncia caracterizada por comprometimento da memria episdica. Os resultados do
suporte para existncia de amplo espectro de disfunes associadas ao envelhecimento, em pacientes com PD. No
foram demonstradas correlaes significativas com tempo de doena.
Palavras-chave: doena de Parkinson, demncia, idade.
This study was conducted at the Universidade Estadual Paulista, Faculdade de Medicina Botucatu, Departamento de Neurologia, Psicologia and Psiquiatria, Botucatu
SP, Brazil.
1
Universidade Estadual Paulista, Faculdade de Medicina Botucatu, Departamento de Neurologia, Psicologia and Psiquiatria, Botucatu SP, Brazil. 2Servio de Psicologia, Hospital das Clnicas da Faculdade de Medicina de Botucatu, PS, Brazil. 3Universidade Estadual Paulista, Instituto de Biocincias, Departamento de Estatstica,
Botucatu SP, Brazil. 4Residente de Neurologia, Faculdade de Medicina Botucatu, SP, Brazil. 5Servio de Reabilitao, Hospital das Clinicas da Faculdade de Medicina
de Botucatu, SP, Brazil.
Arthur Oscar Schelp. Departamento Neurologia / Psicologia e Psiquiatria / Faculdade Medicina de Botucatu / UNESP Rubio Jr, S/N 18618-970 Botucatu
SP Brazil. E-mail: aschelp@fmb.unesp.br
Disclosure: The authors report no conflicts of interest.
Received May 05, 2016. Accepted in final form July 11, 2016.
204 Episodic memory in Parkinsons disease Schelp et al.
INTRODUCTION
ncreasing patient life expectancies call for a greater

understanding of the influence of age on the different
dysfunctions that occur over the course of degenerative
diseases. Ageing is one of the well-defined risk factors
for the incidence of dementia in patients with Parkinsons disease (PD).1,2 PD could itself be a result of ageing.3 Some cohort series show an incidence for dementia
with PD (PDD) of over 65%, with the relative risk being
5.1 times that of controls.4,5 In patients with PD, advancing age is associated with worsening of motor symptoms
and a lowering of response to medical treatment.6 The
relationship between motor symptoms and cognitive deficits in PD is also well established.7,8 The broad
spectrum of cognitive disorders observed in different
phases of the development of PD,9 including cognitive
patterns associated with Lewy Body Dementia (LBD)
and Alzheimers disease (AD), supports the hypothesis
that other distinct pathologies may be superimposed
on symptoms associated with PDD.10,11 Some evidence
supports the existence of a greater prevalence of nonsynuclein-related symptoms with advancing age.12 Compromised episodic memory is a hallmark symptom of
AD and has a well-demonstrated association with ageing.13 The identification of particular forms of cognitive
deterioration may contribute to the understanding of
the relationship among the dementia spectrum, ageing,
and PD. The aim of the present study was to analyse the
association between dementia associated with delayed
recall memory dysfunction in PD patients and demographic variables.
METHODS
Study design and procedure. A cross-sectional observa-
tional study was carried out over a 2-year period in

patients diagnosed with PD and being treated at the
Outpatient Unit for Movement Disorders at the Clinicas Hospital of Botucatu Medical School, Sao Paulo,
Brazil. The Research Ethics Committee of Botucatu
Medical School, So Paulo State University, approved
the study. All participants, or their legal guardians,
provided written informed consent.
A two-stage protocol was applied. Initially, the
patients were evaluated using the Brief Cognitive Battery (BBRC-Edu)14 (screening tests for detecting the
presence of cognitive impairment). Subsequently,
those patients in whom memory impairment was identified were evaluated by a specific instrument, the Mattis Dementia Rating Scale (MDRS), validated for the
Brazilian population.15 The BBRC-Edu included tests
of visual perception (naming of ten simple drawings),
incidental and immediate memory, learning, verbal fluency, delayed recall (after 5 min), and recognition tasks
(recognition of ten familiar figures presented among
new ones). Specialized psychologists applied the test. If
the patients were in the ON or extreme OFF phase, the
tests were repeated at another date and time, and only
this second evaluation was included in the analysis. The
patients with episodic memory compromise (delayed
recall with cut-off score 7), were classified as instances
of dementia. The MDRS includes five subscales of distinct cognitive domains: attention, initiative/perseverance, construction, conceptualization and memory, with
a cut-off score of 122. Socio-demographic (sex, age, and
formal education level) and clinical history (diagnosis
and treatment time) data were collected.
Selection and description of participants.Over a period
of two consecutive years, 125 patients were selected

randomly for inclusion in the study. The inclusion
criteria were: subjects under supervised care for at least
1 year with a diagnosis of PD, and aged over 18 years.
The exclusion criteria were a prior history of stroke,
atypical PD, vitamin B12 deficiency, or metabolic
encephalopathy.
Statistical analysis. Although in this observational
cross-sectional study causal relationships could not be
evaluated, the variables were classified as: i) predictive
variables, ii) confounding variables, and iii) outcomes.
We estimated the possible effects of double and triple
interactions between variables on the occurrence of
dementia.
Descriptive measures were obtained for quantitative
and qualitative variables, and a comparison was made
between groups (case and non-case) using Students
t-test. Considering episodic memory as a response variable, a regression model was fitted with age, educational
level and time since diagnosis as explanatory variables.
All analyses were carried out using Statistical Analysis
Software (SAS) for Windows v.9.3. The significance level
was set at 5% for the tests applied.
RESULTS
Among the 125 patients studied, 12 did not finish the
proposed analysis, giving a total of 113 patients, of
which 63.6% were male. The mean age of the sample
was 68.099.43 years and the mean formal education
level was 3.913.23 years. The mean length of time
since the patients developed PD was 7.675.22 years.
Tables 1 and 2 depict patient socio-demographic data
and results on the screening battery of sub-tests. A
Schelp et al.Episodic memory in Parkinsons disease 205
significant difference was observed between the group

of patient not exhibiting compromised memory on the
screening subtests (no case) and the group exhibiting
impairment (case). This difference was in relation to
age (p0.001) and for scores on all screening battery
subtests (p0.001), except for the identification/
naming subtest (Table 2). Tables 3 and 4 show the correlations of performance with age and formal education.
Thus, age was negatively correlated with performance
on the scale (p=0.0094) whereas formal education was
positively correlated (p=0.0797) both with the applied
screening test and the MDRS. Table 5 shows the age
correlation with the MDRS subscales. No correlation
with disease duration was found (Tables 3 and 4).
DISCUSSION
The socio-demographic characteristics of the sample
studied (Table 1) are similar to those of the general
elderly population in Brazil,16 except for the predominance of males in the group. This could be explained by
the fact that PD is more prevalent in men of advanced
age.17 Formal education is relevant to the present
study, since it was associated with worse results on the
subtests (Table 2). As has been observed elsewhere,18
formal education is markedly deficient in Brazil.
Some studies call attention to the heterogeneous
pattern of cognitive dysfunction in patients newly diagnosed with PD.19 The question of whether there is a type
of dementia specifically associated with PD remains a
Table 1. Descriptive measures of socio-demographic variables and performance on sub-tests.

Variables
Socio-demographic variables
Performance on
screening sub-tests
MeanSD
Minimum
Maximum
Median
Age
68.099.43
113
42.00
83.00
70.00
Formal education (years)
3.913.23
93
0.00
15.00
4.00
Time since diagnosis
7.675.22
111
1.00
23.00
6.00
Identification/Naming
9.711.26
110
1.00
10.00
10.00
Incidental memory
5.141.80
110
0.00
9.00
5.00
Immediate memory
6.552.32
110
0.00
10.00
7.00
Learning
7.272.32
110
0.00
10.00
8.00
Delayed recall
6.152.82
110
0.00
10.00
7.00
Recognition
8.352.71
110
0.00
10.00
9.50
SD: standard deviation.
Table 2. Comparison between groups (occurrence and non-occurrence of dementia).

Non-occurrence
(n=67)
Occurrence
(n=46)
p-value*
Age
64.949.68
72.676.90
<0.0001
4.383.42
3.322.92
0.0874
7.454.98
7.915.40
0.7692
Identification/naming
9.751.23
9,641.32
0.3760
Incidental memory
5.691.52
4.331.88
0.0001
Immediate memory
7.491.96
5.202.15
0.0001
Learning
8.371.76
5.692.11
0.0001
Delayed recall
7.632.04
4.022.41
0.0001
Recognition
9.421.41
6.803.35
0.0001
Variables
Socio-demographic variables
Performance on screening sub-tests
*t-test for independent samples.
Table 3. Model of multiple linear regression for performance on BBRCEdu (dependent variable 5 min.
recall memory).
Variables
Estimate
Std. Error
pvalue
Intercept
14.19824
3.74899
0.0005
Age
0.13981
0.05100
0.0094
0.20501
0.11375
0.0797
0.07230
0.06131
0.2459
Table 4. Model of multiple linear regression for performance on MDRS.

Variables
Estimate
Std. Error
pvalue
Intercept
208.10242
37.74367
<.0.0001
Age
1.57871
0.51344
0.0039
2.58489
1.14519
0.0300
0.69516
0.61728
0.2673
matter of debate. Although it is difficult to differentiate

LBD and AD in PDD, it is nonetheless accepted that each
presents a distinct pattern of cognitive impairment.11,12
The screening test used to identify patients affected
by episodic memory dysfunction includes evaluation of
incidental, immediate memory, delayed recall and recognition. The brief battery of tests shows good specificity and sensitivity when used in populations with a low
level of education.20 Tests of delayed recall memory are
highly accurate detectors of dementia in AD.21 On the
other hand, immediate recall, as measured by word-list
tests, is less accurate in distinguishing patients with
very mild AD from normal healthy controls.22 The use
of pictures to detect disturbances in delayed recall is still
regarded as the gold standard for assessing memory in
a wide range of aged individuals.23
The analysis revealed a significant relationship
between age and a dementia that involves compromised
episodic memory, as determined by the screening test
(Table 2). With the exception of visual perception and
naming, all other memory assessments showed deficits
(p0.0001). The Mattis evaluation (Tables 4 and 5) confirmed the results of the screening test, showing compromise across all domains. The age correlation indicates
that the older the patient, the lower the Mattis sub-test
scores, reflecting a homogeneous worsening of cognitive
skills with aging in PD demented patients.
The demonstration of a relationship between dementia and ageing in patients with PD corroborate the
results of other studies.1,4,5 An earlier study reported a
wide spectrum of impairments in neuropsychological
function emerging with ageing, including, in particular, dementia associated with memory dysfunction.2
In the cited report, patients with late onset Parkinsonism performed worse than those with early onset in
all memory functions, particularly in picture completion and associative learning (Wechsler memory scale
I). Another study failed to find differences in memory
impairment among an early and late-onset group, compared with age-matched controls24 and questioned the
possibility of concomitant AD pathology. However, the
fact that episodic memory dysfunction is significantly
correlated with aging in patients with PD reinforces the
hypothesis that dementia involving memory deterioration during PD could result from concurrent AD. The
existence of two cognitive syndromes of PD was outlined by a previous cohort study;25 PD may involve two
distinct cognitive syndromes that evolve independently,
with the dementia related to an increase in tau protein
transcription, and effects on dopaminergic structures
associated with frontal-executive disorders. Dementia
was diagnosed in patients with a Mini-Mental State
Examination (MMSE) score of 2.27 After 7.9 years of
follow-up, the data showed a persistent strong statistical
Table 5. Spearman Correlation between age and cognitive impairment.

Mattis Sub-tests
Attention
Initiation and perseveration
Construction
Conceptualization
Memory
Total
0.41
0.50
0.50
0.37
0.35
0.50
0.014
0.002
0.002
0.028
0.038
0.002
correlation between ageing and impaired performance

on a task of verbal and semantic fluency.26 Since the
study defined dementia using a verbal task, the disruption should be considered one of semantic rather than
episodic memory. On the other hand, a meta-analysis of
verbal fluency deficits in patients with PD failed to demonstrate any qualitative difference between demented
and non-demented patients.27
The test of visual perception and naming showed no
marked differences between the memory-compromised
and unimpaired groups (Tables 2 and 3). As stated in a
recent review,28 visual perception may be less intrinsically related to learning than to reward-related phenomena like motivation and attention. It is reasonable to
suppose that when a learning test was given, motivation
and attention were higher than in the initial moments
of neuropsychological evaluations that demonstrated
memory disturbances. Identification and naming can
be influenced by semantic memory and other cognitive functions, and do not specifically evaluate episodic
memory. It should also be remembered that this was a
cross-sectional study, including individuals at different
stages of the disease, with various kinds of disturbed
memory function, including problems with working and
semantic memory. The role of distinct cerebral structures in the incidence and progression of PD dementia
remains a matter of debate. The demonstration that
only axial impairment was correlated with age, whereas
dementia incidence was associated with bradykinesia and speech, suggests that both dopaminergic and
non-dopaminergic structures are involved in the etiopathogenesis of dementia in PD.7 Hornykiewicz et al.,
in 1984,29 reported that concurrent cortical noradrenaline and cholinergic function deficiencies, as well as
basal ganglia dopamine deficiency are key factors in the
development of dementia in PD. The indications that
dopaminergic structures may be associated with frontal-executive disorders that develop independently,25
offer clues to distinguishing different forms of cognitive deterioration in PD. To understand the phenotypic
diversity of dementia associated with PD, it is crucial
to consider the possibility of subgroups, identified by

pathogenesis and aetiology.30 This is reasonable considering the varied cognitive disabilities that appear during
the course of PD. Although recent studies indicate that
at least two distinct forms of cognitive dysfunction arise
as PD progresses, the current study shows no evidence
of distinct sub-groups suffering from a compromise of
frontal or anterior cortical function. Caution must be
exercised in interpreting our results. A cross-sectional
study minimizes the impact of the data collected. On the
other hand, it provides additional evidence supporting
the hypothesis that dementia in PD, when initially associated with memory disturbances, develops in distinct
ways that worsen with advancing age.
The present study, focused on cognitive deterioration, corroborates the hypothesis that at least one distinctive form of cognitive impairment can be attributed
to PD. This data should be validated with longitudinal
studies and larger samples including other variables.
The novel on-going studies investigating the molecular
genetics and pathogenesis of PD, should shed new light
on how to identify distinct subgroups of patients, each
of which may require a specific therapeutic approach and
prognosis.
Author contribution. Arthur Oscar Schelp: design,
analyse, intellectual contribution to the writing of the

manuscript. Cristiane Lara Mendes-Chiloff: analyse,
intellectual contribution to the writing of the manuscript. Vanessa Cristina Paduan: analyse, intellectual
contribution to the writing of the manuscript. Jos
Eduardo Corrente: analyse, intellectual contribution to
the writing of the manuscript. Fabrcio Diniz de Lima:
Intellectual contribution to the writing of the manuscript. Juliana Cristine Nunes Marchette: analyse,
intellectual contribution to the writing of the manuscript. Gustavo Jos Luvizuto: intellectual contribution
to the writing of the manuscript. Rodrigo Bazan: intellectual contribution to the writing of the manuscript.
Support. FAPESP- 2012 11394-7. So Paulo, Brazil.
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Dement Neuropsychol 2016 September;10(3):204-209